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Myocardial Infarction for USMLE Step 3

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Myocardial Infarction for the USMLE Step 3 Exam
Myocardial infarction (MI), commonly called a heart attack, results from prolonged ischemia and subsequent myocardial cell death due to an acute reduction in coronary blood flow. MI is typically caused by atherosclerotic plaque rupture with thrombus formation, leading to either complete or partial occlusion of a coronary artery. MIs are classified into ST-segment elevation MI (STEMI) and non-ST-segment elevation MI (NSTEMI) based on ECG findings and clinical presentation.
Pathophysiology
  • Atherosclerosis: Chronic plaque buildup within coronary arteries narrows the lumen, reducing blood flow. Plaques can have lipid-rich cores and thin fibrous caps that make them prone to rupture.
  • Plaque Rupture and Thrombus Formation: When a plaque ruptures, the exposed lipid core activates platelets and the coagulation cascade, resulting in thrombus formation. A thrombus can lead to partial or complete occlusion of the coronary artery.
  • Ischemia and Infarction: Prolonged ischemia leads to irreversible myocardial cell death. In STEMI, ischemia typically affects the full thickness (transmural) of the myocardium; in NSTEMI, it is limited to the subendocardium.
Risk Factors
  • Modifiable: Smoking, hypertension, hyperlipidemia, diabetes, obesity, sedentary lifestyle, and diet.
  • Non-Modifiable: Age, race, sex, family history of early CAD. Risk is higher in African Americans than in White Americans. Women have higher mortality than men.
Clinical Presentation
myocardial infarction signs and symptoms
  • Chest Pain: A common symptom, often described as a squeezing or crushing sensation in the central chest, radiating to the left arm, jaw, neck, or back. The pain lasts over 20 minutes and may not resolve with rest.
  • Associated Symptoms: Diaphoresis, nausea, vomiting, dyspnea, and anxiety.
  • Additional Presentations: Common in women, older adults, and diabetics, with symptoms such as fatigue, syncope, or abdominal pain.
Types of Myocardial Infarction
ST-Segment Elevation Myocardial Infarction (STEMI)
  • Definition: Characterized by full-thickness myocardial infarction with ST-segment elevation on ECG.
  • Diagnosis:
    • ECG: ST-segment elevation in two or more contiguous leads, indicating transmural ischemia.
    • Biomarkers: Elevated troponins confirm myocardial injury.
  • Management:
    • Reperfusion Therapy:
    • Primary PCI: Preferred within 90 minutes of first medical contact.
    • Fibrinolysis: Administered if PCI is unavailable within 120 minutes, ideally within 30 minutes of presentation.
    • Medications: Aspirin, P2Y12 inhibitors (e.g., clopidogrel), heparin, beta-blockers, ACE inhibitors, and statins.
Non-ST Segment Elevation Myocardial Infarction (NSTEMI)
  • Definition: Subendocardial infarction without ST-segment elevation, diagnosed by elevated troponins.
  • Diagnosis:
    • ECG: ST depression, T-wave inversion, or nonspecific changes.
    • Biomarkers: Elevated troponins confirm myocardial injury.
  • Management:
    • Medications: Dual antiplatelet therapy (aspirin and P2Y12 inhibitor), anticoagulation, beta-blockers, ACE inhibitors, and high-intensity statins.
    • Risk Stratification: Use TIMI or GRACE scores to guide invasive management, with PCI for high-risk patients.
Complications of Myocardial Infarction
  • Early Complications (first 24–72 hours):
    • Arrhythmias: Ventricular fibrillation, tachycardia, atrial fibrillation, or bradycardia.
    • Heart Failure: Due to left ventricular dysfunction.
    • Cardiogenic Shock: Severe hypotension and poor perfusion.
  • Mechanical Complications (days to weeks post-MI):
    • Papillary Muscle Rupture: Leads to acute mitral regurgitation.
    • Ventricular Septal Rupture: Causes a new murmur and hemodynamic instability.
    • Free Wall Rupture: Results in cardiac tamponade, often fatal.
  • Late Complications:
    • Left Ventricular Aneurysm: Can cause persistent ST elevation and potential thrombus formation.
    • Pericarditis: Presents as chest pain; often self-limited or occurring as part of Dressler’s syndrome.
Key Points
  • Pathophysiology: MI results from atherosclerotic plaque rupture and thrombus formation, leading to ischemia and cell death.
  • Types of MI:
    • STEMI: Complete coronary occlusion with ST-segment elevation; requires immediate reperfusion with PCI or fibrinolysis.
    • NSTEMI: Partial occlusion; managed with antithrombotic therapy and risk-based PCI.
  • Diagnosis:
    • ECG: ST elevation in STEMI; ST depression or T-wave inversion in NSTEMI.
    • Biomarkers: Elevated troponins confirm myocardial injury in both STEMI and NSTEMI.
  • Management:
    • STEMI: Requires immediate reperfusion with PCI or fibrinolysis.
    • NSTEMI: Dual antiplatelet therapy, anticoagulation, and beta-blockers; PCI in high-risk cases.
  • Complications:
    • Early: Arrhythmias, heart failure, and cardiogenic shock.
    • Mechanical: Papillary muscle rupture, ventricular septal rupture, and free wall rupture.
    • Late: Left ventricular aneurysm and pericarditis.

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